From the Departments of Medicine (Cardiac Unit), Radiology, and Nuclear
Medicine, Massachusetts General Hospital, Harvard Medical School, Boston,
Mass.
Correspondence to Henry Gewirtz, MD, Cardiac Unit/Vincent Burnham 3, Massachusetts General Hospital, Boston, MA 02114. E-mail gewirtz.henry{at}mgh.harvard.edu
BackgroundWe tested the
hypothesis that correction of hyperlipidemia improves
coronary vasodilator response and maximal perfusion in
myocardial regions having substantial impairment of pretreatment
vasodilator capacity.
Methods and ResultsMeasurements of myocardial blood flow
were made with PET [13N]ammonia in 12 patients with
ischemic heart disease (11 men; age, 65±8 years [mean±SD])
at rest and during adenosine at 70 and then 140 µg ·
kg-1 · min-1 for 5 minutes each before
and
ConclusionsShort-term lipid-lowering therapy increases
stenotic segment maximal myocardial blood flow by
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Effects of Short-Term Treatment of Hyperlipidemia on Coronary Vasodilator Function and Myocardial Perfusion in Regions Having Substantial Impairment of Baseline Dilator Reverse
4 months after simvastatin treatment (40 mg daily).
Simvastatin reduced LDL (171±13 before versus 99±18 mg/dL
after simvastatin, P<0.001) and increased
HDL (39±8 versus 45±9 mg/dL, P<0.05). Myocardial
segments were classified on the basis of pretreatment blood flow
response to 140 µg · kg-1 ·
min-1 adenosine as normal (flow
2 mL ·
min-1 · g-1) or abnormal (flow <2
mL · min-1 · g-1). In normal
segments, baseline myocardial blood flow (0.95±0.32) increased
(P<0.001) at both low- (1.62±0.81) and high-
(2.63±0.41) dose adenosine and was unchanged both at rest and
with adenosine after simvastatin. In abnormal
segments, myocardial blood flow at rest (0.73±0.19) increased at low-
(1.06±0.59, P<0.02) and high- (1.29±0.33,
P<0.01) dose adenosine. After
simvastatin, myocardial blood flow increased more compared
with pretreatment at both low- (1.37±0.66, P<0.05
versus pretreatment) and high- (1.89±0.79, P<0.01
versus pretreatment) dose adenosine.
45%. The
mechanism involves enhanced, flow-mediated dilation of stenotic
epicardial conduit vessels and may account at least in part for the
efficacy of lipid lowering in secondary prevention trials and in
reducing ischemic episodes in ambulatory patients.
Key Words: blood flow ischemia heart diseases simvastatin
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